Rescue of follicle development after oocyte-induced ovary dysfunction and infertility in a model of POI

The mechanisms and aetiology underlying the development of premature ovarian insufficiency (POI) are poorly understood. However, oocyte clearly has a role as demonstrated by Double Mutant (DM) mouse model where dysfunction (6 weeks) is followed POI (3 months) due to oocyte-specific deletion complex hybrid N- O-glycans. ovaries DM mice contain more primary follicles (3a stage) accompanied fewer developing follicles, indicating block in follicle development. To investigate this block, we first analysed early postnatal (8-day), pre-pubertal (3-week) post-pubertal (6-week 3-month) ( C1galt1 F/F Mgat1 :ZP3 Cre ) Control mice. Second, investigated if transplantation into “normal” endocrine environment would restore Third, determined replacing somatic cells rescue oocytes. At 3-week, 3a large oocytes second GC layer increased proliferation. 6-week, abnormally oocytes, with decreased Transplantation ‘normal’ did not normal generating reaggregated (ROs) enable progress thus highlighted intra-ovarian factors were responsible for onset females. Thus, these studies demonstrate oocyte-initiated altered communication between GCs results abnormal which fail leads POI.